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EN4.{12-14,16-20} | Hearing Vestibular and Neuro Otology — Graded Quiz
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Which of the following correctly describes Rinne's test result in a patient with pure conductive hearing loss?
Correct. In conductive hearing loss, the middle ear mechanism is impaired, so air-conducted sound is attenuated. Bone-conducted sound bypasses the middle ear and is heard better, making BC > AC — a Rinne NEGATIVE result.
Rinne NEGATIVE (BC > AC) = conductive hearing loss. Rinne POSITIVE (AC > BC) = normal OR sensorineural loss. This definition is absolute — do not invert.
Rinne positive (AC > BC) is the normal finding and also occurs in sensorineural loss. Conductive loss always produces Rinne negative (BC > AC). There is no clinical category of 'Rinne equivocal.'
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In Weber's test, a 512 Hz tuning fork placed on the vertex lateralises to the right ear in a patient with a history of right ear discharge and perforation. This finding is consistent with:
Correct. A perforated TM causes right-sided conductive hearing loss. In CHL, Weber lateralises TO the affected ear because the masking effect of ambient noise is reduced on that side, allowing the bone-conducted vibration to be perceived more strongly.
Weber lateralises TO the affected ear in conductive loss (background noise is masked on the side with CHL, so bone-conducted vibration is perceived louder there). Weber lateralises AWAY from the affected ear in SNHL (the damaged cochlea perceives less). Right discharge + perforation = conductive loss → Weber to the right.
Weber lateralises AWAY from the affected ear in SNHL, not towards it. Weber lateralising to the right indicates either right-sided conductive loss OR left-sided SNHL. Given the right ear history, right CHL is the correct interpretation.
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A 50-year-old woman reports episodic attacks of severe rotatory vertigo lasting 2–4 hours, low-pitched tinnitus in the left ear, and fluctuating left-sided hearing loss. She has noticed her hearing is worse during attacks and improves between them. The PATHOPHYSIOLOGICAL basis of her condition is:
Correct. Meniere's disease results from endolymphatic hydrops — abnormal accumulation of endolymph in the scala media. The resulting pressure build-up and periodic rupture of Reissner's membrane (mixing endo- and perilymph) produces the characteristic attacks of vertigo + fluctuating low-frequency SNHL + tinnitus.
Meniere's disease is caused by endolymphatic hydrops — excess endolymph distends the membranous labyrinth and periodically ruptures Reissner's membrane, mixing endo- and perilymph. The low-frequency fluctuating SNHL, episodic vertigo, tinnitus and aural fullness are hallmarks. Viral vestibular neuritis, canalolithiasis (BPPV), and stapes fixation (otosclerosis) are distinct entities.
Viral inflammation of the vestibular nerve (A) = vestibular neuritis — a single prolonged attack without auditory symptoms. Canalolithiasis (C) is the mechanism of BPPV — free-floating otoconia in the SCC causing brief positional vertigo with no hearing loss. Stapes fixation (D) = otosclerosis — conductive hearing loss, no vertigo.
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A 40-year-old patient presents with a 2-year history of progressive unilateral right-sided hearing loss. Audiometry shows: right ear — bone conduction thresholds 5 dB across all frequencies; air conduction thresholds 45 dB at 500 Hz, 40 dB at 1000 Hz, with Carhart notch at 2000 Hz. Left ear is normal. Tympanometry shows absent stapedial reflexes on the right. The most likely diagnosis is:
Correct. Otosclerosis shows: normal bone conduction (cochlea intact), large air-bone gap (conductive loss from stapes fixation), absent stapedial reflexes (fixed stapes cannot vibrate), and Carhart notch at 2 kHz. No ear discharge and a normal TM (unless Schwartze sign is present) complete the picture. Definitive treatment is stapedectomy.
Otosclerosis: progressive conductive loss (large AC-BC air-bone gap), normal bone conduction, absent stapedial reflexes (stapes fixed), Carhart notch at 2 kHz (mechanical artefact), and normal TM. The combination of normal BC, absent reflexes, and Carhart notch is diagnostic. NIHL = SNHL with 4 kHz notch; CSOM = perforation + discharge.
SNHL (A) would show reduced BONE conduction, not normal BC with a large AB gap. CSOM (C) requires TM perforation and ear discharge. NIHL (D) causes bilateral SNHL with a 4 kHz notch — no air-bone gap, not unilateral, and absent stapedial reflexes are not a feature.
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A 32-year-old man presents to the emergency department following a temporal bone fracture in a road traffic accident. He has complete right facial palsy, deafness, and haemotympanum on the right. The fracture runs along the long axis of the petrous bone. This type of fracture is:
Correct. Longitudinal temporal bone fractures run parallel to the long axis of the petrous bone and account for ~80% of cases. They typically cause haemotympanum, conductive hearing loss, and TM lacerations. Facial nerve involvement occurs in ~20% (compared to ~50% in transverse fractures). Transverse fractures more often damage the cochlea (SNHL) and facial nerve.
Longitudinal fractures run along the long axis of the petrous bone (commonest, ~80%), typically cause haemotympanum + conductive hearing loss; facial nerve involved in ~20%. Transverse fractures run perpendicular to the long axis (~20% of cases), more often injure the facial nerve (~50%) and cause SNHL (cochlea/IAC disruption). This patient has a longitudinal fracture (long axis); the facial palsy and SNHL may co-occur but facial nerve involvement is less typical.
Transverse fractures (A, D) are LESS common (~20%) and more frequently injure the facial nerve (~50%) and cochlea. The fracture described here runs along the long axis — longitudinal, the commonest type.
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A 23-year-old male engineering graduate presents with bilateral high-frequency hearing loss. He has worked in a factory with machinery noise for 5 years and did not use ear protection. Audiometry shows a characteristic bilateral symmetrical sensorineural hearing loss with a notch at which frequency?
Correct. The 4 kHz notch is pathognomonic of NIHL. The outer hair cells at the basal cochlear turn (high-frequency region, ~4 kHz) are maximally vulnerable to acoustic trauma, producing the characteristic audiometric notch.
Noise-induced hearing loss (NIHL) characteristically produces a bilateral symmetrical SNHL with a notch at 4000 Hz (4 kHz). This reflects selective damage to outer hair cells at the basal turn of the cochlea, which are tuned to ~4 kHz. The notch at 4 kHz with relative recovery at 8 kHz is pathognomonic of acoustic trauma.
250 Hz (A) is low-frequency — damaged in Meniere's disease, not NIHL. 1 kHz (B) is mid-frequency — not the characteristic NIHL notch. 8 kHz (D) is affected in advanced NIHL but the defining notch is at 4 kHz, with relative recovery at 8 kHz.
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A 4-year-old boy is brought with suspected hearing loss identified at school. BERA (auditory brainstem response) shows bilateral absent waves. The SINGLE most important initial investigation to determine treatment candidacy is:
Correct. The first priority in a deaf child is to quantify and characterise the hearing loss using ABR (BERA) and OAEs — to determine candidacy for hearing aids or cochlear implantation. Imaging follows to assess cochlear anatomy, and genetics determines aetiology.
For a deaf child, management begins with confirming the DEGREE and TYPE of hearing loss (ABR/BERA establishes threshold and morphology; OAEs assess outer hair cell function). Only after this can a decision be made about hearing aids vs cochlear implantation. Imaging (CT/MRI) is important but follows audiological characterisation for candidacy.
CT temporal bone (A) assesses cochlear anatomy for cochlear implant candidacy but comes AFTER audiological confirmation. MRI IAC (B) is also important for implant planning but is not the first step. Genetic counselling alone (D) without audiological workup cannot guide management decisions about amplification or surgery.
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A patient undergoes audiometry showing: right ear — air conduction 45 dB, bone conduction 45 dB; left ear — air conduction 10 dB, bone conduction 10 dB. The Absolute Bone Conduction (ABC) test would show which of the following in the right ear?
Correct. The audiogram shows no air-bone gap in the right ear (both AC and BC at 45 dB), confirming SNHL. In SNHL, cochlear function is impaired. The ABC test reflects cochlear reserve — in SNHL the patient perceives bone-conducted sound for less time than a normal examiner, i.e. ABC is reduced.
ABC (absolute bone conduction) compares the patient's bone conduction with the examiner's (assumed normal). In SNHL the cochlea is damaged, so bone conduction is REDUCED — the patient hears the tuning fork for a shorter duration than the examiner. In pure conductive loss, the cochlea is intact and ABC is normal. Here the audiogram shows equal AB thresholds (no AB gap) = SNHL, so ABC is reduced.
ABC is normal in pure CONDUCTIVE loss (cochlea intact). In SNHL (as here, with no AB gap), the cochlea is impaired and ABC is reduced. It does not require Weber to be interpreted.
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During Dix-Hallpike manoeuvre, the patient is moved from sitting to supine with the head turned 45° to the right and hanging 30° below the horizontal. After a latency of 5 seconds, the patient develops severe vertigo and nystagmus with upbeat-torsional components. The nystagmus fatigues on repeat testing. The most likely involved structure is:
Correct. Dix-Hallpike with head turned right places the RIGHT posterior SCC in the dependent (gravity-sensitive) position. Displaced otoconia (canalolithiasis) in this canal produce upbeat-torsional nystagmus with latency and fatigability — the hallmark of BPPV. The right posterior SCC is the most commonly affected canal in BPPV.
Dix-Hallpike with the head turned to the RIGHT tests the RIGHT posterior SCC. Positive result = upbeat-torsional nystagmus with a latency of 5–30 seconds that fatigues on repeated testing (canalolithiasis). The fast phase of nystagmus beats towards the affected (dependent) ear. This is the classic presentation of BPPV affecting the right posterior SCC — the commonest canal affected.
The horizontal SCC is tested by the roll test (supine head roll), not Dix-Hallpike. Anterior SCC BPPV is rare and produces down-beat nystagmus. The utricle's otoconia that are displaced cause BPPV in the SCCs — isolated utricular pathology does not produce Dix-Hallpike positional nystagmus.
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A 55-year-old woman is diagnosed with Meniere's disease affecting the right ear. She has had four disabling attacks in the past 6 months despite maximum medical therapy (low-salt diet, betahistine, diuretics). Which of the following is the appropriate NEXT step in management?
Correct. Intratympanic gentamicin (chemical labyrinthectomy) is the appropriate second-line intervention for refractory Meniere's disease when medical management fails. It selectively ablates the vestibular neuroepithelium of the affected ear, eliminating the source of attacks. The risk is hearing loss in the treated ear.
When medical management (low-salt diet, betahistine, diuretics) fails in Meniere's disease, the next step is intratympanic gentamicin — chemical labyrinthectomy of the affected ear. It ablates the vestibular function of the diseased labyrinth, preventing attacks at the cost of some hearing loss risk. Epley's is for BPPV. Cochlear implants treat bilateral profound SNHL, not Meniere's. Increasing betahistine is not evidence-based for refractory disease.
Simply increasing betahistine (A) is not a validated strategy for medically refractory Meniere's. Epley's manoeuvre (C) treats BPPV — displaced otoconia — not endolymphatic hydrops; it is entirely wrong here. Bilateral cochlear implantation (D) is for bilateral profound SNHL and is not indicated here.
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